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Genome-wide expression profiling analysis of a Hmgn1, 3 and 5 mutant mouse model

ABSTRACT: Members of the HMGN protein family bind to nucleosomes and affect chromatin structure and functions as transcription, replication and DNA repair as well as epigenetic modifications. Overexpression of Hmgn1 may be linked to the etiology of Down syndrome while underexpression may be linked to some leukemias. Hmgn3 is highly expressed in eye and in brain and might influence behavioral phenotype. For Hmgn5 effects on transcription levels e.g. in liver are suggested. Total RNA obtained from four homozygote mutant and wildtype male mice were compared.

ORGANISM(S): Mus musculus

SUBMITTER: Marion Horsch 

PROVIDER: E-GEOD-39062 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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High mobility group N proteins modulate the fidelity of the cellular transcriptional profile in a tissue- and variant-specific manner.

Kugler Jamie E JE   Horsch Marion M   Huang Di D   Furusawa Takashi T   Rochman Mark M   Garrett Lillian L   Becker Lore L   Bohla Alexander A   Hölter Sabine M SM   Prehn Cornelia C   Rathkolb Birgit B   Racz Ildikó I   Aguilar-Pimentel Juan Antonio JA   Adler Thure T   Adamski Jerzy J   Beckers Johannes J   Busch Dirk H DH   Eickelberg Oliver O   Klopstock Thomas T   Ollert Markus M   Stöger Tobias T   Wolf Eckhard E   Wurst Wolfgang W   Yildirim Ali Önder AÖ   Zimmer Andreas A   Gailus-Durner Valérie V   Fuchs Helmut H   Hrabě de Angelis Martin M   Garfinkel Benny B   Orly Joseph J   Ovcharenko Ivan I   Bustin Michael M  

The Journal of biological chemistry 20130424 23

The nuclei of most vertebrate cells contain members of the high mobility group N (HMGN) protein family, which bind specifically to nucleosome core particles and affect chromatin structure and function, including transcription. Here, we study the biological role of this protein family by systematic analysis of phenotypes and tissue transcription profiles in mice lacking functional HMGN variants. Phenotypic analysis of Hmgn1(tm1/tm1), Hmgn3(tm1/tm1), and Hmgn5(tm1/tm1) mice and their wild type lit  ...[more]

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